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Blood, 15 June 2005, Vol. 105, No. 12, pp. 4849-4852. Prepublished online as a Blood First Edition Paper on February 15, 2005; DOI 10.1182/blood-2004-12-4897. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-12-4897v1 105/12/4849    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by De Keersmaecker, K. Articles by Cools, J. Search for Related Content PubMed PubMed Citation Articles by De Keersmaecker, K. Articles by Cools, J. Related Collections Neoplasia Oncogenes and Tumor Suppressors Brief Reports Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief report Fusion of EML1 to ABL1 in T-cell acute lymphoblastic leukemia with cryptic t(9;14)(q34;q32) Kim De Keersmaecker, Carlos Graux, Maria D. Odero, Nicole Mentens, Riet Somers, Johan Maertens, Iwona Wlodarska, Peter Vandenberghe, Anne Hagemeijer, Peter Marynen, and Jan Cools From the Department of Human Genetics, Flanders Interuniversity Institute for Biotechnology (VIB), Leuven, Belgium; Departments of Human Genetics and Hematology, University of Leuven, Leuven, Belgium; and Department of Genetics, University of Navarra, Pamplona, Spain. The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL). We recently identified NUP214-ABL1 as a variant ABL1 fusion gene in 6% of T-ALL patients. Here we describe the identification of another ABL1 fusion, EML1-ABL1, in a T-ALL patient with a cryptic t(9;14)(q34;q32) associated with deletion of CDKN2A (p16) and expression of TLX1 (HOX11). Echinoderm microtubule-associated protein-like 1-Abelson 1 (EML1-ABL1) is a constitutively phosphorylated tyrosine kinase that transforms Ba/F3 cells to growth factor-independent growth through activation of survival and proliferation pathways, including extracellular signal-related kinase 1/2 (Erk1/2), signal transducers and activators of transcription 5 (Stat5), and Lyn kinase. Deletion of the coiled-coil domain of EML1 abrogated the transforming properties of the fusion kinase. EML1-ABL1 and breakpoint cluster region (BCR)-ABL1 were equally sensitive to the tyrosine kinase inhibitor imatinib. These data further demonstrate the involvement of ABL1 fusions in the pathogenesis of T-ALL and identify EML1-ABL1 as a novel therapeutic target of imatinib. (Blood. 2005;105:4849-4852) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: A remarkABL new fusion oncogene in T-cell ALL Richard A. Van Etten Blood 2005 105: 4547-4548. [Full Text] [PDF] This article has been cited by other articles: S. Mustjoki, S. Hernesniemi, A. Rauhala, M. Kahkonen, A. Almqvist, T. Lundan, and K. Porkka A novel dasatinib-sensitive RCSD1-ABL1 fusion transcript in chemotherapy-refractory adult pre-B lymphoblastic leukemia with t(1;9)(q24;q34) Haematologica, October 1, 2009; 94(10): 1469 - 1471. [Full Text] [PDF] S. Chiaretti and R. Foa T-cell acute lymphoblastic leukemia Haematologica, February 1, 2009; 94(2): 160 - 162. [Full Text] [PDF] K. De Keersmaecker, I. Lahortiga, N. Mentens, C. Folens, L. Van Neste, S. Bekaert, P. Vandenberghe, M. 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Schwartz NUP214-ABL1 in adult T-ALL: the GMALL study group experience Blood, November 15, 2006; 108(10): 3556 - 3559. [Abstract] [Full Text] [PDF] E. Bremer, B. t. Cate, D. F. Samplonius, L. F. M. H. de Leij, and W. Helfrich CD7-restricted activation of Fas-mediated apoptosis: a novel therapeutic approach for acute T-cell leukemia Blood, April 1, 2006; 107(7): 2863 - 2870. [Abstract] [Full Text] [PDF]

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